alexa The role of interleukin 18 in the pathogenesis of hypertension-induced vascular disease.
Cardiology

Cardiology

Journal of Clinical & Experimental Cardiology

Author(s): Rabkin SW

Abstract Share this page

Abstract Understanding the mechanism by which chronic high blood pressure induces vascular disease is of fundamental importance for prevention of the adverse consequences of hypertension. Clinical and population studies have consistently found increased circulating levels of interleukin 18 (IL-18) in patients with hypertension. Although obesity, and possibly age, is a determinant of plasma IL-18 levels, the relationship of IL-18 to hypertension seems to be independent of these factors. Experimental evidence indicates that the expression of IL-18 and/or its receptor can be induced by catecholamines or angiotensin, two factors that are involved in the pathophysiology of hypertension. Elevated circulating IL-18 levels are associated with vascular changes in the carotid artery, including increased carotid intima-media thickness, which, in turn, is a predictor of cardiovascular events in patients with established coronary disease. IL-18, either directly or through oxidative stress pathways and matrix metalloproteins, can alter endothelial function or induce vascular smooth muscle cell migration and/or proliferation to produce the vascular changes that occur with hypertension. This Review examines the data on IL-18 and hypertensive vascular disease, and explores the potential cellular and molecular mechanisms that might connect hypertension to vascular disease. This article was published in Nat Clin Pract Cardiovasc Med and referenced in Journal of Clinical & Experimental Cardiology

Relevant Expert PPTs

Relevant Speaker PPTs

  • Alsayed Alnahal
    Urinary netrin-1 predict early ischemic acute kidney injury after cardiopulmonary bypass
    PPT Version | PDF Version
  • Donald silverberg
    Is correction of iron deficiency a new addition to the treatment of heart failure?
    PPT Version | PDF Version
  • Ahmed Zeidan
    Effects of intravenous iron in chronic kidney disease and heart failure
    PPT Version | PDF Version
  • Ming Yang
    Generation, characterization and application of monoclonal antibodies against foot-and-mouth disease virus serotype A
    PPT Version | PDF Version
  • Jan Voskuil
    How antibodies can prevent medical progress and how they can be great tools?
    PPT Version | PDF Version
  • Ekaterina Rogaeva
    Mutation analysis of CHCHD10 in neurodegenerative diseases, including Parkinson’s disease
    PPT Version | PDF Version
  • Alexandra Vatsiou
    Pathways and genes under positive selection in metabolic diseases
    PPT Version | PDF Version
  • Yosef Yarden
    Classically, the 3’untranslated region (3’UTR) is that region in eukaryotic protein-coding genes from the translation termination codon to the polyA signal. It is transcribed as an integral part of the mRNA encoded by the gene. However, there exists another kind of RNA, which consists of the 3’UTR alone, without all other elements in mRNA such as 5’UTR and coding region. The importance of independent 3’UTR RNA (referred as I3’UTR) was prompted by results of artificially introducing such RNA species into malignant mammalian cells. Since 1991, we found that the middle part of the 3’UTR of the human nuclear factor for interleukin-6 (NF-IL6) or C/EBP gene exerted tumor suppression effect in vivo. Our subsequent studies showed that transfection of C/EBP 3’UTR led to down-regulation of several genes favorable for malignancy and to up-regulation of some genes favorable for phenotypic reversion. Also, it was shown that the sequences near the termini of the C/EBP 3’UTR were important for its tumor suppression activity. Then, the C/EBP 3’UTR was found to directly inhibit the phosphorylation activity of protein kinase CPKC in SMMC-7721, a hepatocarcinoma cell line. Recently, an AU-rich region in the C/EBP 3’UTR was found also to be responsible for its tumor suppression. Recently we have also found evidence that the independent C/EBP 3’UTR RNA is actually exists in human tissues, such as fetal liver and heart, pregnant uterus, senescent fibroblasts etc. Through 1990’s to 2000’s, world scientists found several 3’UTR RNAs that functioned as artificial independent RNAs in cancer cells and resulted in tumor suppression. Interestingly, majority of genes for these RNAs have promoter-like structures in their 3’UTR regions, although the existence of their transcribed products as independent 3’UTR RNAs is still to be confirmed. Our studies indicate that the independent 3’UTR RNA is a novel non-coding RNA species whose function should be the regulation not of the expression of their original mRNA, but of some essential life activities of the cell as a whole.
    PPT Version | PDF Version
  • Inga Zemite
    Fungal diseases of the scalp skin in the trichologist practice
    PPT Version | PDF Version
  • Juan Manuel Navarrete
    “Juan Manuel Navarrete-National-University-of-México-Mexico-Fulvi-H-as-posible-treatment-for-viral-diseases”
    PPT Version | PDF Version
  • Sariya Mohammadi
    Case Series Of Rare Breast Diseases And Their Unusual Presentation
    PPT Version | PDF Version
  • David Jamil Hadad
    METHODOLOGY TO COLLECT SPUTUM SPECIMENS
    PPT Version | PDF Version
  • Ferdinand N Mbagwu
    Ethnomedical studies of plants used for treatment of diseases in eastern part of Nigeria
    PPT Version | PDF Version
  • K Lakshmi
    Common diseases encountered in back yard poultry
    PPT Version | PDF Version
  • Sarah E Cavanaugh
    Alcoholism and mental illness: overlapping diseases requiring a renewed focus
    PPT Version | PDF Version

Recommended Conferences

Relevant Topics

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords